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Orthopedics > Basic Sciences: Section 1 Bone > Flashcards

Basic Sciences: Section 1 Bone Flashcards

1
Q

Endocrine effects on bone healing:

Cortisone

A

Negative, decreased callus proliferation

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2
Q

Endocrine effects on bone healing:

Calcitonin

A

Positive(?), Unknown

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3
Q

Endocrine effects on bone healing:

TH, PTH

A

Positive, Bone remodeling

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4
Q

Endocrine effects on bone healing:

GH

A

Positive, increased callus formation

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5
Q

Stages of graft healing

A
  1. Inflammation, chemotaxis
  2. Osteoblast differentiation
  3. Osteoinduction
  4. Osteoconduction
  5. Remodeling, continues for years
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6
Q

Under optimal stability what type of frature healing takes place?

A

Intramembranous ossification

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7
Q

Under instability what type of frature healing takes place?

A

Enchondral ossification

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8
Q

Under extreme instability what type of frature healing takes place?

A

Pseudoarthrosis

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9
Q

Three histologic phases of distraction osteogenesis?

A
  1. Latency Phase, 5-7 days, no distraction
  2. Distraction Phase, 1mm/day, 1 inch/month
  3. Consolidation Phase, 2x longer than distraction phase
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10
Q

Dietary requirment of Calcium in children?

A

600 mg/day

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11
Q

Dietary requirment of Calcium in adolescents and young adults (10-25)?

A

1300mg/day

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12
Q

Mechanism of PTH

A
  • cAMP
  • decreased serum calcium stimulates Beta-2 receptors to release PTH.
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13
Q

Mechanism of Calcitonin

A
  1. Increased serum Ca cause secretion of Calcitonin by parafollicular clear cells of the thyroid gland
  2. Controlled by Beta-2 receptors
  3. Inhibits osteoCLAST resorption
  4. decreases serum Ca
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14
Q

Hypercalcemia symptoms

A
  1. Polyuria
  2. Polydypsia
  3. Kidney stones
  4. Excessive bony resorption
  5. CNS effects - confusion, stupor, weakness
  6. Constipation
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15
Q

Primary hyperparathyroidism

A
  • Overproduction of PTH (parathyroid adenoma MC)
  • Increased osteoclastic resorption
  • High Ca, PTH, Alk phos, and urinary phos
  • Low serum phos
  • Brown tumors
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16
Q

Pseudohypoparathyroidism (PHP)

A
  • PTH receptor abnormality, PTH has no effect - blocked by cAMP pathway or lack of cofactors (Mg)
  • PTH is normal or high
  • Low Ca, High Phos
  • Genetic disorder
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17
Q

Albrights hereditary osteodystrophy

A
  • Form of pseudohypoparathyroidism
  • PTH receptor abnormality
  • Short 1st, 4th, 5th metacarpals/tarsals (brachydactyly)
  • Exostosis
  • Obesity
  • MR
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18
Q

Pseudo-pseudohypoparathyroidism

(pseudo-PHP)

A
  • Phenotype of PHP
  • PTH response is normal
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19
Q

Renal osteodystrohpy:

High-turnover

A
  • Kidney disease:
    • Decreased phosphate excretion –> very high serum Phos –> decrease Ca –> very high PTH –> SECONDARY HYPERPARATHYROIDISM
  • Rugger Jersey spine, osteitis fibrosa, amyloidosis
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20
Q

Renal osteodystrohpy:

Low-turnover

A
  • Normal PTH, elevated Ca and normal Phos
  • Due to aluminum deposition in bones which
    • decreases mineralization of bone
    • decreases proliferation of osteoblasts
    • impairs release of PTH from parathyroid glands
  • Rugger Jersey spine, osteitis fibrosa, amyloidosis
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21
Q

Sustained increase in PTH (secondary hyperparathyroidism) is caused by which mechanisms?

A
  • Diminished renal excretion of Phosphorus
  • Hypocalcemia
  • Impaired Calcitriol
  • Altered control of PTH release
  • Skeletal resistance to PTH
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22
Q

Phosphorus retention causes PTH secretion in what three ways?

A
  1. Phos binds to serum calcium –> hypocalcemia –> increaed PTH production
  2. Phos impairs 1-alpha-hydroxylase–> decrease production of active vitamin D–> increase PTH
  3. Phos direct stimulation of PTH synthesis
23
Q

Rickets:

Vitamin D deficiency

A
  • Insufficient Vit D in diet/malabsorbtion
  • Bone deformities and hypotonia
  • Rachitic Rosary (enlarged costochondral junction)
  • Wide growth plates
  • decrease Ca and Phos
  • High PTH and Alk phos
  • Physeal widening/cupping on Xray
24
Q

Rickets:

Vitamin D dependant

A
  • Type I - pseudo-vitamin D deficiency
    • Very low active Vit D (1-alpha hydroxylase is defective)
    • Osteomalacia
  • Type II
    • Very high active Vit D (Vit D receptor defective)
    • Osteomalacia
    • Alopecia
    • Poor mineralization
25
Q

Rickets:

Vitamin D resistent

A
  • AKA hypophosphatemic rickets
  • MC form
  • Decrease renal tubular phosphate resoprtion –> Phos spilling into urine
  • Vit D iis inappropriatly normal
  • Classic triad
    1. Hypophosphatemia
    2. Lower limb deformities
    3. Stunted growth rate
26
Q

Hypophosphatasia

A
  • Caused by very low alkaline phosphatase
  • Bone deformities and hypotonia
  • Early loss of teeth
  • Osteomalacia
  • Elevated urine phosphoethanolamine is diagnostic
27
Q

Scurvy

A
  • Vitamin C deficiency –> decrease chondroitin sulfate synthesis –> defective collagen
  • BLEEDING (gums, effusions, ecchymosis) –> iron def. –> fatigue
  • Thin cortices
  • Corner sign (metaphyseal clefts)
  • Osteopenia
  • Widening zone of provisional calcification
28
Q

Paget’s disease

A
  • Osteoclastic abnormality –> increased bone turnover
  • Bone deformities –> fractures, pain, CHF
  • “Picture frame vertabrae”
  • High serum Alk Phos
  • High urinary hydroxyproline levels
  • Virus-like inclusion bodies in osteoclasts
  • Phases
    • Active
      • Lytic - osteoclastic bone resorbtion
      • Mixed
      • Sclerotic - osteoblastic bone formation
    • Inactive
29
Q

Hyperthyroidism

A
  • Hypermetabolism –> increased bone turnover –> High Ca
  • Normal Phos, Alk Phos, Vit D and PTH
  • Increased free thryroxin
  • Decreased TSH
30
Q

Vitamin D intoxication

A
  • Vitamin D cross reacts with intestines –> increasd absorption of Ca
  • High Ca and very high Vitamin D
  • Tachy, tremors
31
Q

Hypoparathyroidism

A
  • Decreased Ca and increased Phos
  • Basal ganglia calcification
  • MC cause is iatrogenic
32
Q

Osteoporosis

A
  • Type I
    • postmenopausal
    • affects trabecular/cancellous bone
  • Type II
    • age-related
    • affects BOTH cortical and trabecular bone
  • Tx with 1000-1500 mg Ca and 400-800 IU of Vit D per day
33
Q

Idiopathic transient osteoporosis of the hip

A
  • uncommon
  • most common in 3rd trimester or pregnancy, can occur in men as well
  • localized osteopenia without hx of trauma
  • self-limiting, resolves within 6-8 months (this differentiates it from osteonecrosis)
34
Q

Osteomalacia

A
  • qualitative defect - mineralization issue
  • Caused by:
    • Vit D deficient diet
    • GI disorders of absorbtion
    • Renal osteodystrophy
    • Drugs
      • antacids (contain aluminum)
      • Phynytoin
    • Alcoholism
  • Xrays
    • Looser’s zone fractures
35
Q

Osteogenesis imperfecta

A
  • Glycine substitution in procollagen –> failure of collagen cross-linking –> Type I collagen mutation
36
Q

Lead poisoning

A
  • Short stature
  • Decreased bone density
  • Altered chondrocyte response to PTH-related protein and TGF-B
37
Q

Osteopetrosis

A
  • Marble bone disease
  • Impaired osteoclast/chondroclast function (no ruffled border or clear zone) –> failure of bone resorption –> sclerosis and obliteration of the mudullary canal
  • Infantile AR form
    • more severe, hepatosplenomegaly, aplasastic anemia
  • AD “tarda” form
    • generalized osteosclerosis, rugger jersey spine
38
Q

Osteopoikilosis

A
  • Spotted bone disease
  • Islands of deep cortical bone appear within the medullary cavity and cancellous bone of the long bones
    • hands/feet MC
39
Q

Osteonecrosis

A
  • Death of bone not caused by infection
  • Typically caused by loss of blood supply - Hip MC
  • A/w
    • Chronic steroid use
    • Alcoholism
    • Sickle cell disease
    • Dysbarism (caisson’s disease)
    • Radiation therapy
    • Gaucher’s disease
  • Histologic chronology
    • autolysis of osteocytes and necrotic marrow –> inflammation of invasion of new mesenchymal cells –> new woven bone over top dead trabeculae –> resorption of dead trabeculae –> COLLAPSE (sometimes)
40
Q

Chandler’s disease

A

Osteonecrosis of femoral head in adults

41
Q

Osteochondrosis:

Van Neck’s disease

A

ischiopubic synchondrosis

4-11 years

42
Q

Osteochondrosis:

Legg-Calve-Perthes diseaes

A

Femoral head

4-8 years

43
Q

Osteochondrosis:

Osgood-Schlatter disease

A

Tibial tuberosity

11-15 years

44
Q

Osteochondrosis:

Sinding-Larsen-Johansson syndrome

A

inferior patella

10-14 years

45
Q

Osteochondrosis:

Blount’s disease

A

Proximal tibial epiphysis

1-3 years (infants)

8-15 years (adolescents)

46
Q

Osteochondrosis:

Sever’s disease

A

Calcaneus

9-11 years

47
Q

Osteochondrosis:

Kohler’s disease

A

Tarsal navicular

3-7 years

48
Q

Osteochondrosis:

Freiberg’s infarction

A

Metatarsal head

13-18 years

49
Q

Osteochondrosis:

Scheurmann’s disease

A

Discovertebral junction

13-17 years

50
Q

Osteochondrosis:

Panner’s disease

A

Capitellum of humerus

5-10 years

51
Q

Osteochondrosis:

Thiemann’s disease

A

Phalanges of hand

11-19 years

52
Q

Osteochondrosis:

Keinbock’s disease

A

Carpal lunate

20-40 years

53
Q
A

Orthopedics (5 decks)

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